Alzheimer's disease is a neurodegenerative disease pathologically characterized by neuronal degeneration and loss as well as formation of senile plaques and neurofibrillary tangles. Alzheimer's disease causes cognitive symptoms which progressively destroy memory, recognition, thinking, judgment, and the like, eventually leading to death.
A principal protein constituting the senile plaques deposited in the brain is amyloid β peptide (Aβ), which consists of 39 to 43 amino acids. Aβ exhibits cytotoxicity, and this cytotoxicity is considered to cause Alzheimer's disease (Non Patent Literature 1). Aβ secreted from cells is a polypeptide consisting mainly of 40 or 42 amino acids. Particularly, Aβ consisting of 42 amino acids is known to have a stronger aggregability leading to its earlier deposition in the brain, and stronger cytotoxicity (Non Patent Literature 2). Thus, an agent for inhibiting Aβ aggregation has been expected as a prophylactic or therapeutic agent for Alzheimer's disease.
L-[Lys-Leu-Val-Phe-Phe], a partial sequence of Aβ, is known to have aggregation inhibitory activity against Aβ (Non Patent Literature 3).